scholarly journals Nuclear Transport: A Switch for the Oxidative Stress—Signaling Circuit?

2012 ◽  
Vol 2012 ◽  
pp. 1-18 ◽  
Author(s):  
Mohamed Kodiha ◽  
Ursula Stochaj
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Stress Response ◽  
Nuclear Transport ◽  
Stress Signaling ◽  
Oxygen Species ◽  
Nuclear Trafficking ◽  
The Impact ◽  
Transport Of Macromolecules ◽  
Signaling Circuit

Imbalances in the formation and clearance of reactive oxygen species (ROS) can lead to oxidative stress and subsequent changes that affect all aspects of physiology. To limit and repair the damage generated by ROS, cells have developed a multitude of responses. A hallmark of these responses is the activation of signaling pathways that modulate the function of downstream targets in different cellular locations. To this end, critical steps of the stress response that occur in the nucleus and cytoplasm have to be coordinated, which makes the proper communication between both compartments mandatory. Here, we discuss the interdependence of ROS-mediated signaling and the transport of macromolecules across the nuclear envelope. We highlight examples of oxidant-dependent nuclear trafficking and describe the impact of oxidative stress on the transport apparatus. Our paper concludes by proposing a cellular circuit of ROS-induced signaling, nuclear transport and repair.

Overproduction of NOX-derived ROS in AML promotes proliferation and is associated with defective oxidative stress signaling

Blood ◽  
2013 ◽  
Vol 122 (19) ◽  
pp. 3322-3330 ◽  
Author(s):  
Paul S. Hole ◽  
Joanna Zabkiewicz ◽  
Chinmay Munje ◽  
Zarabeth Newton ◽  
Lorna Pearn ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Stress Response ◽  
Reactive Oxygen ◽  
Oxidative Stress Response ◽  
Antioxidant Defenses ◽  
Stress Signaling ◽  
Oxygen Species ◽  
Key Points ◽  
P38mapk Signaling

Key Points More than 60% of primary AML blasts constitutively produce high levels of NOX-derived reactive oxygen species (ROS), which drives AML proliferation. High ROS AMLs show depleted antioxidant defenses but evade the oxidative stress response through suppression of p38MAPK signaling.

Intrathymic and intrasplenic oxidative stress mediates thymocyte and splenocyte damage in acutely exercised mice

1999 ◽  
Vol 86 (6) ◽  
pp. 1823-1827 ◽  
Author(s):  
A. A. Azenabor ◽  
L. Hoffman-Goetz
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Acute Exercise ◽  
Lipid Peroxides ◽  
Membrane Lipid ◽  
Splenic Tissue ◽  
Lymphoid Tissues ◽  
Oxygen Species ◽  
The Impact

Reactive oxygen species may contribute to apoptosis in lymphoid tissues observed after exercise. Thymic and splenic tissues excised from control mice (C) or mice immediately after ( t 0) or 24 h after ( t 24) a run to exhaustion (RTE) were assayed for biochemical indexes of oxidative stress [thymic and splenic membrane lipid peroxides, superoxide dismutase, catalase, plasma uric acid (UA), and ascorbic acid (AA)]. There were significant increases in membrane lipid peroxides in thymus ( P < 0.001) and spleen ( P < 0.001) in acutely exercised mice relative to controls (thymus: C = 2.74 ± 0.80 μM; t 0 = 7.45 ± 0.48 μM; t 24 = 9.44 ±1.41 μM; spleen: C = 0.48 ± 0.22 μM; t 0 = 1.78 ± 0.28 μM; t 24 = 2.81 ± 0.34 μM). The thymic and splenic tissue antioxidant enzymes concentrations of superoxide dismutase and catalase were significantly lower in samples collected at t 0 relative to C and t 24 mice ( P < 0.001). Plasma UA and AA levels were used to assess the impact of the RTE on the peripheral antioxidant pool. There was no significant change in UA levels and a significant reduction in plasma AA concentrations ( P < 0.001); the reduction in plasma AA occurred at t 24 (6.53 ± 1.64 μM) relative to t 0 (13.11 ± 0.71 μM) and C (13.26 ± 1.2 μM). These results suggest that oxidative damage occurs in lymphoid tissues after RTE exercise and that such damage may contribute to lymphocyte damage observed after acute exercise.

Oxidative stress and cardiovascular health: therapeutic potential of polyphenols

2013 ◽  
Vol 91 (3) ◽  
pp. 198-212 ◽  
Author(s):  
Sandhya Khurana ◽  
Matthew Piche ◽  
Amanda Hollingsworth ◽  
Krishnan Venkataraman ◽  
T.C. Tai
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Recent Progress ◽  
Cardiovascular Health ◽  
Therapeutic Potential ◽  
Cellular Function ◽  
Oxygen Species ◽  
The Impact ◽  
Detrimental Impact ◽  
Normal Cellular Function

Reactive oxygen species (ROS) are important in normal cellular function and physiology. However, oxidative stress resulting from an accumulation of ROS has a detrimental impact on cellular function, and ROS has been implicated in the pathogenesis of a number of diseases, including cardiovascular diseases. This review provides a summary of the impact of ROS on cardiovascular health and diseases, highlighting the therapeutic use of antioxidants. In addition, this review summarizes the health benefits of polyphenols, and the recent progress on understanding the cellular and physiological actions by which polyphenols may impart their beneficial properties on cardiovascular health.

scholarly journals The copper chaperone CcsA coupling with superoxide dismutase SodA mediates oxidative stress response in Aspergillus fumigatus

2021 ◽  
Author(s):  
Wenlong Du ◽  
Pengfei Zhai ◽  
Shuai Liu ◽  
Yuanwei Zhang ◽  
Ling Lu
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Stress Response ◽  
Aspergillus Fumigatus ◽  
Fungal Pathogens ◽  
Oxidative Stress Response ◽  
Superoxide Dismutases ◽  
Oxygen Species ◽  
Oxidative Response

Superoxide dismutases (SODs) are important metalloenzymes that protect fungal pathogens against the toxic effects of reactive oxygen species (ROS) generated by host defense mechanisms during the infection process. The activation of Cu/Zn-SOD1 is found to be dependent on its c haperone Ccs1 ( c opper c haperone for S OD1). However, the role of Ccs1 ortholog in the human pathogen Aspergillus fumigatus and how these SODs coordinate to mediate oxidative stress response remain elusive. Here, we demonstrated that A. fumigatus CcsA, a Saccharomyces cerevisiae Ccs1 ortholog, is required for cells in response to oxidative response and the activation of Sod1. Deletion of ccsA resulted in increased ROS accumulation and enhanced sensitivity to oxidative stress due to loss of SodA activity. Molecular characterization of CcsA revealed that the conserved CXC motif is required not only for the physical interaction with SodA but also for the oxidative stress adaption. Notably, addition of Mn 2+ or overexpression of cytoplasmic Mn-SodC could rescue the defects of the ccsA or sodA deletion mutant, indicating the important role of Mn 2+ and Mn-SodC in ROS detoxification; however, deletion of CcsA-SodA complex could not affect A. fumigatus virulence. Collectively, our findings demonstrate that CcsA functions as a Cu/Zn-Sod1 chaperone that participates in the adaptation to oxidative stress in A. fumigatus and provide a better understanding of the CcsA-SodA complex-mediated oxidative stress response in filamentous fungi. IMPORTANCE Reactive oxygen species (ROS) produced by phagocytes have been reported to participate in the killing of fungal pathogens. Superoxide dismutases (SODs) are considered to be the first defense line against superoxide anions. Characterizing the regulatory mechanisms of SOD activation is important for understanding how fungi adapt to oxidative stress in hosts. Our findings demonstrated that CcsA functions as a SodA chaperone in A. fumigatus and that the conserved CXC motif within CcsA is required for its interaction with SodA and the CcsA-SodA-mediated oxidative response. These data may provide new insights into how fungal pathogens adapt to oxidative stress via the CcsA-SodA complex.

scholarly journals The impact of reactive oxygen species in the development of cardiometabolic disorders: a review

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Roland Akhigbe ◽  
Ayodeji Ajayi
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Reactive Oxygen ◽  
Acid Oxidation ◽  
Ros Generation ◽  
Metabolic Memory ◽  
Oxygen Species ◽  
Cardiometabolic Disorders ◽  
The Impact

AbstractOxidative stress, an alteration in the balance between reactive oxygen species (ROS) generation and antioxidant buffering capacity, has been implicated in the pathogenesis of cardiometabolic disorders (CMD). At physiological levels, ROS functions as signalling mediators, regulates various physiological functions such as the growth, proliferation, and migration endothelial cells (EC) and smooth muscle cells (SMC); formation and development of new blood vessels; EC and SMC regulated death; vascular tone; host defence; and genomic stability. However, at excessive levels, it causes a deviation in the redox state, mediates the development of CMD. Multiple mechanisms account for the rise in the production of free radicals in the heart. These include mitochondrial dysfunction and uncoupling, increased fatty acid oxidation, exaggerated activity of nicotinamide adenine dinucleotide phosphate oxidase (NOX), reduced antioxidant capacity, and cardiac metabolic memory. The purpose of this study is to discuss the link between oxidative stress and the aetiopathogenesis of CMD and highlight associated mechanisms. Oxidative stress plays a vital role in the development of obesity and dyslipidaemia, insulin resistance and diabetes, hypertension via various mechanisms associated with ROS-led inflammatory response and endothelial dysfunction.

scholarly journals Positive feedback between ROS and cis-axis of PIASxα/p38α-SUMOylation/MK2 facilitates gastric cancer metastasis

2021 ◽  
Vol 12 (11) ◽  
Author(s):  
Qian Wang ◽  
Ci Xu ◽  
Qiang Fan ◽  
Haihua Yuan ◽  
Xin Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gastric Cancer ◽  
Reactive Oxygen Species ◽  
Stress Response ◽  
Cancer Cells ◽  
Regulatory Mechanism ◽  
Reactive Oxygen ◽  
Oxidative Stress Response ◽  
Oxygen Species ◽  
Gastric Cancer Cells

AbstractMAPK/p38 is an important mammalian signaling cascade that responds to a variety of intracellular or extracellular stimuli, such as reactive oxygen species (ROS), and participates in numerous physiological and pathological processes. However, the biological function of p38 in different tumors, and even at different stages of the same tumor, remains elusive. To further understand the regulatory mechanism of p38 and oxidative stress in the occurrence and development of gastric cancer, we report SUMOylation as a novel post-translational modification occurring on lysine 152 of MAPK14/p38α through immunoprecipitation and series of pull-down assays in vitro and in vivo. Importantly, we determine that p38α-SUMOylation functions as an authentic sensor and accelerator of reactive oxygen species generation via interaction with and activation of MK2 in the nucleus, and the ROS accumulation, in turn, promotes the SUMOylation of p38α by stabilizing the PIASxα protein. This precise regulatory mechanism is exploited by gastric cancer cells to create an internal environment for survival and, ultimately, metastasis. This study reveals novel insights into p38α-SUMOylation and its association with the intracellular oxidative stress response, which is closely related to the processes of gastric cancer. Furthermore, the PIASxα/p38α-SUMOylation/MK2 cis-axis may serve as a desirable therapeutic target in gastric cancer as targeting PIASxα, MK2, or a specific peptide region of p38α may reconcile the aberrant oxidative stress response in gastric cancer cells.

scholarly journals Reactive Oxygen Species (ROS), Oxidative Stress and its role In HIV Infection

2020 ◽  
Vol 11 (3) ◽  
pp. 4560-4568
Author(s):  
Sunita S Patil ◽  
Vaishali S Patil ◽  
Arvind Gulbake
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Hiv Infection ◽  
Critical Role ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Hiv Patients ◽  
Signalling Molecules ◽  
The Impact

Throughout several regular cell cycles, reactive oxygen species (ROS) play a critical role. When ROS values are high, and when the defence mechanism (antioxidants) cannot neutralise, they harm and modify the part of biological molecules. They also act as signalling molecules which generate a spectrum of disease.In this study, we reviewed existing oxidants, oxidative stress, and their relationship with infection by human immunodeficiency virus in patients, and the effects of oxidative stress in patients with HIV.Our prospect is to do a clinical study on HIV patients and estimate oxidative parameters like nitric oxide, total antioxidant level and correlate them with CD4 count and viral load which may be helpful during monitoring and giving efficient ART to the HIV patients. And also the importance of ROS in infection has been established through clinical and in vitro studies. Here we review the role of oxidative stress in HIV pathogenesis, the impact of ROS on immune responses in HIV patients, and ROS-mediated regulation of HIV infection. Future studies on the interplay between ROS and HIV infection may offer a new strategy for prevention and treatment.

COPPER AS AN ANSWER ON THE IMPACT OF OXYDESS STRESS ON THE EYES

2018 ◽  
Vol 172 (52) ◽  
pp. 23-28
Author(s):  
Katarzyna Kempka ◽  
Piotr Kamiński ◽  
Grażyna Malukiewicz ◽  
Maria Bogdzińska
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Environmental Conditions ◽  
Defense Mechanisms ◽  
Chemical Elements ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
State Of Emergency ◽  
The Impact ◽  
And Oxidative Stress

The eyes are exposed to many factors, that contribute to the deterioration of their condition. These include environmental conditions and the influence of reactive oxygen species ROS and oxidative stress. Research shows, that one of the most important tasks of created in such way state of emergency is maintenance of relative balance between oxidants (contributing to the formation of ROS) and antioxidants (restraining their effect). Some chemical elements, especially copper, play a key role in blocking ROS and presents an overview of information on the impact of oxidative stress on the eyes and the defense mechanisms with the participation of copper.

Ovariectomy and its Antioxidative Effect on Bone

2010 ◽  
Author(s):  
Durg V. Rai ◽  
Harcharan Singh Ranu
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Bone Loss ◽  
Wistar Rats ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Female Wistar Rats ◽  
The Impact

Ovarian hormone deficiency increases the generation of reactive oxygen species. Oxidative stress due to reactive oxygen species (ROS) can cause oxidative damage to cells. Cells have a number of defense mechanisms to protect themselves from the toxicity of ROS. There is increasing evidence of the role of free radicals in bone resorption and bone loss. Ovariectomised female wistar rats had been used as the animal model for the study of osteoporosis. Even though, there are studies portraying the role of free radicals in bone loss, the defense mechanism adapted by bone in ovariectomised animals remains obscure. So, the impact of ovariectomy on the bone antioxidant system in rats was investigated. Twenty female wistar rats were taken and divided into two groups: ovariectomised and control. It had been found that a significant (p&lt;0.001) decrease in the activity of various enzymes like CAT (catalase), SOD (superoxide dismutase) (p&lt;0.001), GST (glutathione-s-transferase). However, an increase in the malondialdehyde levels was found to be 30% in the ovariectomised rats as compared to the controls. Thus the study elucidates the oxidative stress in bone under ovariectomy.

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